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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Although many genetic variants have been associated with multiple sclerosis (MS) risk, they do not explain all the disease risk and there remains uncertainty as to how these variants contribute to disease.

DNA methylation is an epigenetic mechanism that can influence gene expression and has the potential to mediate the effects of environmental factors on MS.

In a previous study, we found a differentially methylation region (DMR) at MHC <i>HLA-DRB1</i> that was associated within relapsing-remitting MS (RRMS) patients in CD4<sup>+</sup> T cells.

This study aimed to confirm this earlier finding in an independent RRMS cohort of treatment-naïve female patients.

Beta values for all CpGs were analysed using the DMPFinder function in the MINFI program, and a follow-up prioritisation process was applied to identify the most robust MS-associated DMRs.

In addition, we identified a large independent DMR at MHC, whereby 11 CpGs in <i>RNF39</i> were hypermethylated in MS cases compared to controls (max.

CONCLUSIONS: The findings from this study confirm our previous results of a DMR at <i>HLA-DRB1</i> and also suggest hypermethylation in an independent MHC locus, <i>RNF39</i>, is associated with MS<i>.

</i> Taken together, our results highlight the importance of epigenetic factors at the MHC locus in MS independent of treatment, age and sex.

Prospective studies are now required to discern whether methylation at MHC is involved in influencing risk of disease onset or whether the disease itself has altered the methylation profile.

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The Characterization of GSDMB Splicing and Backsplicing Profiles Identifies Novel Isoforms and a Circular RNA That Are Dysregulated in Multiple Sclerosis.

In particular, a growing body of evidence suggests the existence of a pathogenic association between a generalized defect in splicing regulatory genes and multiple sclerosis (MS).

Moreover, several studies have documented an unbalance in alternatively-spliced isoforms in MS patients possibly contributing to the disease etiology.

In this work, using a combination of PCR-based techniques (reverse-transcription (RT)-PCR, fluorescent-competitive, real-time, and digital RT-PCR assays), we investigated the alternatively-spliced gene encoding Gasdermin B, <i>GSDMB</i>, which was repeatedly associated with susceptibility to asthma and AIDs.

Importantly, both AS isoforms and the identified ecircRNA were significantly dysregulated in peripheral blood mononuclear cells of relapsing-remitting MS patients compared to controls, further supporting the notion that aberrant RNA metabolism is a characteristic feature of the disease.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

OBJECTIVE: The aim of this meta-analysis was to undertake a meta-analysis to evaluate the correlation between cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) gene rs221775 A>G single nucleotide polymorphism and the susceptibility of multiple sclerosis (MS) susceptibility.

METHOD: Published manuscripts about CTLA-4 gene rs221775A>G single nucleotide polymorphism and multiple sclerosis susceptibility were searched in the computerized bibliographic searches of Pubmed Embase and China National Knowledge Infrastructure (CNKI).

Potential studies were screened and data for 5025 MS patients and 4706 controls from 20 publications were included.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Genetic variants in the purinergic receptors P2RX4 and P2RX7 have been shown to affect susceptibility to multiple sclerosis (MS).

Sequencing analysis of P2RX4 and P2RX7 in 193 MS patients and 100 controls led to the identification of a rare three variant haplotype (P2RX7 rs140915863:C>T [p.T205M], P2RX7 rs201921967:A>G [p.N361S], and P2RX4 rs765866317:G>A [p.G135S]) segregating with disease in a multi-incident family with six family members diagnosed with MS (logarithm of odds = 3.07).

Our study nominates rare genetic variants in P2RX4 and P2RX7 as major genetic contributors to disease, further supporting a role for these purinergic receptors in MS and the disruption of transmembrane cation channels leading to impairment of phagocytosis as the pathological mechanisms of disease.

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HLA-DRB (human leukocyte antigen-DR beta) alleles, particularly HLA-DRB1*1501, may be of significance in the pathogenesis of MS.

OBJECTIVE: To examine the association of HLA-DRB1*1501 alleles and MBP VNTR (variable number tandem repeat) polymorphism with the MS susceptibility in Iranian population.

The alleles were determined by the Polymerase Chain Reaction (PCR) method in 259 MS patients and 312 healthy control individuals and analyses were carried out using Fisher's exact test.

The two-locus analysis of the interaction between the MBP VNTR polymorphism and the HLA-DRB1 allele showed that the HLADRB1* 1501/A haplotype was more frequent among MS patients than the healthy controls.

CONCLUSION: The interaction between the HLA-DRB1*1501 allele and MBP gene may be considered as a predisposing factor in the development and pathogenesis of MS in the case of gene-gene interaction.

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Based on subsequent reports on the possible involvement of other PPARs and PPARγ coactivator-1alpha (PGC-1α) in neuroinflammation in MS, we analyzed the protein levels of PPARα, PPARβ/δ, and PGC-1α in a subset of CSF samples from the same cohort of relapsing-remitting MS patients.

Unlike PPARγ, none of these proteins were found elevated in MS patients (n=25) compared to non-inflammatory controls (n=16), with the levels of PPARα and PPARβ/δ found generally below the limit of detection, and that of PGC-1α being detectable but comparable in both groups.

The findings suggest that despite their proposed involvement in the regulation of inflammatory processes in MS, PPARα, PPARβ/δ, and PGC-1α proteins are not potential biomarkers of neuroinflammation in MS, and indicate a preferential role of PPARγ in the endogenous regulation of autoimmune response in the human CNS within its receptor family.

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The autoimmune risk gene ZMIZ1 is a vitamin D responsive marker of a molecular phenotype of multiple sclerosis.

: Multiple Sclerosis (MS) is a neurological condition driven in part by immune cells from the peripheral circulation, the targets for current successful therapies.

The autoimmune and MS risk gene ZMIZ1 is underexpressed in blood in people with MS.

Further we show expression is partially heritable (heritability 0.26), relatively stable over time, predominantly in plasmacytoid dendritic cells and non-classical monocytes, and that levels of ZMIZ1 protein expression are reduced in MS.